Abstract
Recent advances in vitamin D research indicate that patients with type 2 diabetes mellitus (T2DM) are suffering from vitamin D deficiency and increased oxidative stress to a variable extent, which could produce different health impacts for each individual. The novel multivariate statistical method applied in the present study allows metabolic phenotyping of T2DM individuals based on vitamin D status, metabolic control, and oxidative stress status in order to identify effectively different subtypes in our type 2 DM study population. Data-driven statistical cluster analysis was performed with 95 patients with T2DM, treated with metformin. Clusters were based on 12 variables—age, disease duration, vitamin D level, insulin, fasting glycemia (FG), glycated hemoglobin (HbA1c), high-density and low-density lipoprotein, total cholesterol (TC), triglycerides (TG), body mass index (BMI), and triglycerides/glucose index (TYG). The analysis revealed four unique clusters which differed significantly in terms of vitamin D status, with a mean 25 (OH) D level in cluster 1 (57.84 ± 11.46 nmol/L) and cluster 4 (53.78 ± 22.36 nmol/L), falling within the insufficiency range. Cluster 2 had the highest mean level of 25 (OH) D (84.55 ± 22.66 nmol/L), indicative of vitamin D sufficiency. Cluster 3 had a mean vitamin D level below 50 nmol/L (49.27 ± 16.95), which is considered deficient. Patients in the vitamin D sufficient cluster had a significantly better glycemic and metabolic control as well as a lower level of lipid peroxidation compared to other clusters. The patients from the vitamin D sufficient cluster also had a significantly higher level of vitamin D/MPO, vitamin D/XO, vitamin D/MDA, vitamin D/CAT, and vitamin D/TRC than that in the vitamin deficient and insufficient clusters. The vitamin D deficient cluster included significantly younger patients and had a significantly lower level of AOPP/TRC and albumin/TRC than the vitamin D sufficient cluster. The evidence from our cluster analysis in the context of separated T2DM demonstrates beneficial effects of optimal vitamin D status on metabolic control and oxidative stress in T2DM patients. Older T2DM patients require higher vitamin D levels in order to achieve good metabolic control and favorable antioxidant protection. Since protein damage is more pronounced in these patients, adding water-soluble antioxidant in addition to higher doses of vitamin D should be considered.
Highlights
Oxidative stress is defined as an imbalance caused by the increased production of free radicals and the inability of cellular antioxidant mechanisms to neutralize these products
Our results showed that vitamin D could have a beneficial anti-inflammatory and antioxidative effect on patients with type 2 diabetes mellitus (T2DM) measured as the vitamin D/MPO ratio because its mean level was significantly higher in vitamin D sufficient than in vitamin D insufficient and deficient clusters
The literature regarding antioxidative effects of vitamin D remained scarce, Nikooyeh et al demonstrated a significant improvement in the MPO activity in 90 T2DM patients supplemented with a 1000 IU fortified vitamin D yoghurt drink daily for four months [49]. Since this enzyme predicts endothelial function in humans and serves as a link among inflammation, oxidative stress, and endothelial dysfunction, our results demonstrated that adequate vitamin D status in patients with T2DM could protect against atherosclerosis [50]
Summary
Oxidative stress is defined as an imbalance caused by the increased production of free radicals and the inability of cellular antioxidant mechanisms to neutralize these products It has been proposed as the root cause of the development of many chronic diseases. Chronic overnutrition and physical inactivity result in lipotoxicity and glucotoxicity, which cause the excessive formation of reactive oxygen species (ROS) and metabolic stress in various organs and tissues including pancreatic β-cells [3]. This is believed to be the main mechanism of the development of insulin. The increased ROS production in T2DM patients activates many detrimental pathways, including the inflammatory pathway involved in cell injury resulting in further disease progression and development of micro- and macrovascular complications [4, 5]
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